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Abstract
Insulin secretion from pancreatic islets is inhibited by the activation of β cell α2A-adrenergic receptors (α2AARs). Increased expression of α2AARs, then, would depress insulin release, which is a pathogenic mechanism of type 2 diabetes. Using congenic rats derived from an inbred model of type 2 diabetes, Rosengren et al. showed that a chromosomal region that includes the gene encoding α2AAR, Adra2a, is associated with increased messenger RNA and protein expression and decreased insulin release. A single-nucleotide polymorphism in the human ADRA2A gene was associated with decreased insulin secretion in normal people during glucose challenge and was also associated with type 2 diabetes. These findings offer another genetic association locus for the disease, with concordant biochemical and expression phenotypes, and also provide a potential new pathway for therapeutic intervention.
Footnotes
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Citation: S. B. Liggett, α2A-Adrenergic receptors in the genetics, pathogenesis, and treatment of type 2 diabetes. Sci. Transl. Med. 1, 12ps15 (2009).
- Copyright © 2009, American Association for the Advancement of Science
